TITLE

Assessing Osteolysis with Use of High-Throughput Protein Chips

AUTHOR(S)
Shanbhag, Arun S.; Kaufman, Adam M.; Hayata, Koichiro; Rubash, Harry E.
PUB. DATE
May 2007
SOURCE
Journal of Bone & Joint Surgery, American Volume;May2007, Vol. 89-A Issue 5, p1081
SOURCE TYPE
Academic Journal
DOC. TYPE
Article
ABSTRACT
Background: Previous studies of bone resorption around failed joint replacements have focused on a limited number of cytokines, primarily tumor necrosis factor-α (TNF-α), interleukin (IL)-1, and IL-6, with use of enzyme-linked immunosorbent assay and immunohistochemistry techniques. In this study, we utilized high-throughput protein chips to profile twenty-nine inflammatory cytokines around failed total joint replacements. Methods: Peri-implant granulomatous tissues were harvested from around the failed total hip prostheses of thirteen patients. Synovial lining capsular tissues from thirteen patients with end-stage degenerative joint disease were used as controls. After homogenization, twenty-nine cytokines were quantified with use of high-throughput protein chips. Results: IL-6 and IL-8 were found consistently in failed joint replacement tissues, reaffirming their prominent role in osteoclastogenesis and end-stage bone resorption. High levels of interferon-γ-inducible protein of 10 kDa (IP-10) and monokine induced by interferon-γ (MIG), both chemoattractants of activated Thi lymphocytes, were also detected. Soluble intercellular adhesion molecule (sICAM) and transforming growth factor-β1 (TGF-β1) were not detected universally, nor were TNF-α or IL-1. After a twenty-four-hour organ culture, IL-1β levels increased substantially along with those of other mediators. We measured but did not detect any activators of cytotoxic T-cells, antibody-producing B-cells, or eosinophils involved in delayed-type hypersensitivity. Variations from patient to patient were seen across all cytokines and highlight the unique response of individual patients to their joint replacements. Conclusions: In failed total joint replacements in patients with end-stage osteolysis, IL-6 and IL-8 may be the primary drivers of osteoclastogenesis. The presence of IP-10 and MIG imply a role for T-cells, while TGF-β1 and sICAM may represent a systemic attempt to modulate the inflammation. TNF-α and IL-1 do not appear to play a major role in the end stages of the disease. Clinical Relevance: These results demonstrate that proteomic tools can provide a foundation for understanding the cytokine-driven osteolysis cascade and a base from which to identify and evaluate potential targets for blockage or augmentation.
ACCESSION #
25019655

 

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